We have developed a simple method for the detection of live spirochaete stages in blood of patients where chronic borreliosis is suspected. Classic techniques involving phase-contrast and fluorescence microscopy are used. The method is also quite sensitive for detecting other bacteria, protists, fungi and other organisms present in blood samples. It is also useful for monitoring the effects of various antibiotics during treatment.

We also present a simple hypothesis for explaining the confusion generated through the interpretation of possible stages of Borrelia seen in human blood. We hypothesize that these various stages in the blood stream are derived from secondarily infected tissues and biofilms in the body with low oxygen concentrations.

Motile stages transform rapidly into cysts or sometimes penetrate other blood cells including red blood cells (RBCs). The latter are ideal hiding places for less motile stages that take advantage of the host’s RBCs blebbing-system. Less motile, morphologically different stages may be passively ejected in the blood plasma from the blebbing RBCs, more or less coated with the host’s membrane proteins which prevents detection by immunological methods.

Ferguson, J., Cure unwanted? Exploring the chronic Lyme disease controversy and why conflicts of interest in practice guidelines may be guidelines guiding us down the wrong path. American Journal of Law and Medicine 2012, 38, 196-224 .

The Lyme Info Net, see especially: Morphological transformation in Borrelia and other spirochetes: Observations of round forms and blebs 1905-2010, see also Survival in adverse conditions. http://www.lymeinfo.net/lymefiles.html

Lyme Disease is a bacterial infection caused by Borrelia Burgdorferi, a spiral-shaped bacteria, or spirochete, transmitted through the bite of an infected tick.

B. burgdorferi is genetically one of the most sophisticated bacteria ever studied. Treponema pallidum (the syphilis spirochete), for example, only has 22 functioning genes whereas the Lyme disease spirochete has 132.

B. burgdorferi changes into three different forms to evade the immune system and antibiotics. The three known forms are the spiral shape (spirochete) that has a cell wall, the cell-wall-deficient form.& the cyst form.

Changing into the cyst form allows the spirochete to hide undetected in the host for months, years or decades until some form of immune suppression occurs, signaling that it is safe for the cysts to open and the spirochetes come out & multiply.

Spirochete- Causative bacteria of Lyme Disease. Spiral shape allows penetration into tissue and bone. Capable of intracellular infection. Rapidly converts to Cell wall deficient and cyst form when threatened by the immune system or antibiotics.

Cell-Wall Deficient (CWD)- Lack of cell wall makes targeting by immune system and antibiotics more difficult. Capable of intracellular infection. Clumps together in colonies―inner layers unreachable by antibiotics and immune system.

Cyst- Dormant form bacteria are not mobile and do not cause symptoms. Can survive antibiotics, starvation, pH changes, temperature changes, and most other adverse conditions. Converts back to spirochete form when conditions are favorable.

Animal studies have shown that in less than a week after being infected, the host can already have the Lyme spirochete deeply embedded inside tendons, muscle, the heart, and even the brain..Once disseminated, B. burgdorferi secludes itself and becomes difficult to detect through testing—and by the immune system.

Borrelia burgdorferi has a replication cycle of about seven days, one of the longest of any known bacteria. Antibiotics are most effective during bacterial replication, so the more cycles during a treatment, the better. Since the life cycle of Streptococcus pyogenes (bacterium that causes strep throat) is about eight hours, antibiotic treatment for a standard 10 days would cover 30 life cycles.

To treat Lyme disease for a comparable number of life cycles, treatment would need to be for at least 30 weeks, providing rationale for doctors who prescribe long-term treatment.

TOP

StrainsThere are 5 subspecies of Borrelia burgdorferi, over 100 strains of Borrelia burgdorferi in the United States and 300 strains worldwide. This diversity is thought to contribute to the antigenic variability of the spirochete and its ability to evade the immune system and antibiotic therapy, leading to chronic infection.

The Borrelia species known to cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato, and have been found to have greater strain diversity than previously thought.

Until recently it was thought that only three genospecies caused Lyme disease:

I. Borrelia burgdorferi sensu stricto (predominant in North America, but also in Europe)

II. Borrelia garinii (predominant in Eurasia)

III. Borrelia afzelii (predominant in Eurasia)

However, newly discovered genospecies have also been found to cause disease in humans:

B. lusitaniae in Europe (especially Portugal), North Africa and Asia, B. bissettii in the U.S. and Europe, and B. spielmanii in Europe. B. valaisiana (Eurasia, especially England, Switzerland and the Netherlands); B. japonica, B. tanukii and B. turdae (Japan); B. sinica, B. andersonii (China); and (U.S.). B. lonestari, recently detected in the Amblyomma americanum tick (Lone Star tick) in the U.S. Suspected of causing STARI. B. miyamotoi spirochete, related to the relapsing fever group of spirochetes, is also suspected of causing illness in Japan.

Note: At present diagnostic tests are based only on B. burgdorferi sensu stricto (the only species used in the U.S.), B. afzelii and B. garinii. Some of these species are carried by ticks not currently recognized as carriers of Lyme disease.

TOPMechanisms of Persistence

B. burgdorferi in sites that are inaccessible to the immune system and antibiotics, such as the brain and central nervous system. New evidence suggests that B. burgdorferi may use the host's fibrinolytic system to penetrate the blood-brain barrier.

Intracellular invasion. B. burgdorferi has been shown to invade a variety of cells, including endothelium, fibroblasts, lymphocytes, macrophages, keratinocytes, and synovium. By 'hiding' inside these cells, B. burgdorferi is able to evade the immune system and is protected to varying degrees against antibiotics, allowing the infection to persist in a chronic state.. Dr. David Dorward from the NIH Rocky Mountain Laboratories, showed that when healthy normal human B-cells were placed in a culture with live Borrelia burgdorferi, that it was only a matter of moments before the spirochetes started to attach and penetrate the anti-body producing white blood cells. Once inside the cell, the bacteria should be killed, but this does not happen. Instead the bacteria actually thrive, and eventually destroy the lymphocyte. Using a time lapse video camera, the spirochete can be seen to enter the B-cell and exit a short distance later, but when it exits it appears to be wearing the membrane of the B-cell.

Antigenic variation. Like the Borrelia that cause relapsing fever, B. burgdorferi has the ability to vary its surface proteins in response to immune attack. This ability is related to the genomic complexity of B. burgdorferi, and is another way B. burgdorferi evades the immune system to establish a chronic infection.

Immune system suppression. Complement inhibition, induction of anti-inflammatory cytokines such as IL-10, and the formation of immune complexes have all been documented in B. burgdorferi infection. .The existence of immune complexes provides another explanation for seronegative disease (i.e. false-negative antibody tests of blood and cerebrospinal fluid), as studies have shown that substantial numbers of seronegative Lyme patients have antibodies bound up in these complexes.